5.2 Chronic Lung Disease, BPD, and Pulmonary Interstitial Emphysema

Chronic Lung Disease, BPD, and Pulmonary Interstitial Emphysema

Quick Answer: Bronchopulmonary dysplasia (BPD) is the usual name for chronic lung disease (CLD) of prematurity. At a nursing level, the definition you will hear most often is ongoing oxygen or positive-pressure need at 36 weeks postmenstrual age (PMA) in an infant born very preterm. Old (classic) BPD was fibrotic injury from high pressure and high oxygen in larger preterms. Current (new) BPD is arrested alveolar growth in extremely preterm infants who may never have had dramatic early barotrauma. Pulmonary interstitial emphysema (PIE) is an air leak of gas into the interstitium along bronchovascular sheaths. Prevention is gentle ventilation, caffeine, nutrition, infection control, and thoughtful patent ductus arteriosus (PDA) management. Postnatal steroids remain controversial; this guide does not invent unpublished AACN doses.

Chronic conditions (CLD/BPD and PIE) are a listed respiratory leaf on the current Neonatal CCRN Test Plan. This OpenExamPrep section is independent nursing-level teaching. It is not a research-methods paper and it is not an AACN medication monograph.

Why two BPD stories exist

Northway’s 1967 description was a moderately preterm or larger infant who survived prolonged mechanical ventilation and then had cystic, fibrotic lungs. That classic BPD histology is airway smooth-muscle hypertrophy, fibrosis, and heterogeneous overdistention. It still happens when a lung is ventilated harshly for days with high FiO2 and high tidal volumes.

New BPD appeared as survival moved to 22–28 weeks. The problem is an incomplete alveolar and microvascular program. Alveoli are fewer and larger (simplified), the interstitium can be cellular, and fibrosis may be modest. The infant may have needed only CPAP and a little oxygen, then still be on 0.25 L nasal cannula at 36 weeks PMA. That infant has chronic lung disease even without a “classic” battle-scarred radiograph.

You do not need to litigate research definitions at the crib, but you should know that teams argue in three languages:

• 36 weeks PMA oxygen or support is the common clinical shorthand and the one families hear.
• The 2001 NIH severity split used at least 28 days of oxygen plus the FiO2 and support mode at 36 weeks PMA (mild = room air at 36 weeks after that oxygen history; moderate = <30% oxygen; severe = ≥30% oxygen and/or positive pressure).
• Jensen 2019 graded severity mainly by support device at 36 weeks PMA (room air = no BPD; low-flow cannula; higher-flow or noninvasive positive pressure; invasive ventilation), de-emphasizing the exact FiO2.

For this exam, remember the 36-week PMA checkpoint and that severity tracks how much hardware the infant still needs, not how scary day 2 looked.

A 24-week infant, now 36 weeks PMA, on 21% oxygen via 1.5 L nasal cannula still meets a commonly used BPD definition. A 34-week infant who needed 3 days of CPAP and is in room air at 36 weeks PMA does not. Do not call every oxygen day after the first week “BPD” in a 35-week infant who is already 36 weeks PMA and in room air.

Numbers that belong in a BPD conversation

Incidence rises steeply below 28 weeks and below 1000 g. Many networks report BPD in a large minority to a majority of survivors at 22–25 weeks, and much lower rates at 30–32 weeks. Those percentages move with definitions, so treat any single published percent as a ballpark, not a score key.

Bedside physiology: former preterms with BPD have high work of breathing, a respiratory rate often 60–80 at rest (quiet term 40–60), expiratory wheeze or noisy secretions, and desaturation with feeds and agitation. Heart rate may sit at 160–180 when the infant is working. Cor pulmonale is the late cardiovascular cost when chronic hypoxemia and high PVR remodel the right ventricle. Link that thought to PPHN teaching, but chronic BPD pulmonary hypertension is not the same as acute transitional PPHN in a term infant with MAS.

Growth is treatment. Calories often need to sit above typical term intakes (many units target a 120–150 kcal/kg/day range in evolving BPD, individualized). Protein supports tissue repair. Fluid overload thickens pulmonary edema. Diuretics are used in some infants for symptomatic edema; they are not a definition of BPD and they do not replace oxygen targeting or calories.

Oxygen targeting in evolving BPD is a unit protocol (many post-acute targets live in the 90–95% band rather than a 99% vanity saturation). Hypoxemia raises PVR. Hyperoxia still injures retina and lung. Follow the written target. A former 25-week infant at 38 weeks PMA who is 84% during every feed is not “a little desat”—that is fuel for pulmonary hypertension and poor growth.

Prevention: what actually moves the curve

Antenatal corticosteroids (an obstetric intervention) and early CPAP with selective surfactant beat routine prolonged high-pressure ventilation. Volume-targeted conventional ventilation and avoidance of hypocapnia reduce volutrauma. Permissive hypercapnia within unit pH limits is a strategy, not an invitation to ignore a pH of 7.15.

Caffeine citrate (loading commonly 20 mg/kg caffeine citrate, maintenance often 5–10 mg/kg/day—follow your protocol) treats apnea and, in the CAP trial world, is associated with less BPD. It is not a steroid and it is not optional trivia. Early caffeine, earlier extubation, and less ventilator time are the mechanistic story.

Nutrition from day 1—protein, calories, human milk when available—supports alveolar growth. Vitamin A prophylaxis appears in some extremely-low-birth-weight protocols; availability and practice vary. Avoid infection and aspiration; both second-hit the developing lung. A former 26-week infant who is “almost out of oxygen” and then aspirates every bottle can look like worsening BPD when the real problem is swallow safety.

PDA contribution: a large left-to-right duct floods the preterm lung, raises ventilator days, and is associated with BPD. Association is not proof that every duct must be closed on day 2. The nursing point is that pulmonary edema from a stealing duct is a modifiable second hit. Bounding pulses, a wide pulse pressure (for example 58/22 mm Hg), a rising oxygen need, and feeding intolerance should send you to the cardiovascular PDA conversation you already studied. Indomethacin, ibuprofen, acetaminophen, device closure, or ligation are tools with gut, kidney, and vocal-cord costs. Here the question is whether the lung is being drowned.

Gentle ventilation checklist you can actually do:

• Smallest effective mean airway pressure; avoid stacked breaths and auto-PEEP.
• Suction only when the tube is obstructed, not every 2 hours by tradition.
• Keep the head midline and the circuit from dragging on the tube.
• Treat pain so the infant is not fighting 30 cm H2O peak pressures.
• Escalate to HFOV when conventional settings are producing PIE or hypoxemia from overdistention rather than from atelectasis.

Pulmonary interstitial emphysema

PIE is gas that has dissected out of alveoli into the interstitium, traveling along bronchovascular bundles. It is an air leak, not an infection. The radiograph shows linear and cystic lucencies, often unilateral at first. The chest can look hyperlucent on the bad side, and the mediastinum may shift. The infant’s saturations fall as compliance falls, and the temptation is to raise MAP—which can pump more gas into the sheaths.

PIE is more common in extremely preterm infants on high MAP, and it can precede pneumothorax. Conceptual moves (unit-specific): reduce tidal trauma, consider HFOV to stabilize MAP with tiny oscillations, position the infant with the more affected side down to reduce ventilation to that lung, and watch for tension physiology. Do not “recruit” a PIE lung the way you recruit a white RDS lung with recruitment maneuvers and more PIP.

Worked example: a 25-week infant on a conventional rate of 60 and a PIP of 28 develops a sudden increase in oxygen from 30% to 70% and a cystic left-lung radiograph. Transillumination is negative. That is PIE until the film says otherwise—not “needs more PIP.” Compare a second infant with the same saturation crash, a dark left chest on transillumination, and shifted heart tones: that is pneumothorax and belongs with pleural-space teaching in section 5.4.

Steroids without a secret dose card

Systemic dexamethasone can extubate some ventilator-dependent infants and may reduce BPD at 36 weeks, but early high-dose dexamethasone is linked to cerebral palsy and neurodevelopmental harm in historical regimens. That is why professional statements have cautioned against routine early high-dose dexamethasone. Later, lower-dose courses, hydrocortisone in selected hypotensive or high-risk extremely preterm infants, and inhaled steroids appear in literature and unit protocols. None of those regimens is published as an AACN CCRN dose. Do not memorize a mg/kg “exam dose” that your unit does not use. The exam-level points are:

• Steroids are a risk-benefit conversation (lung versus brain, infection, hyperglycemia, hypertension, intestinal perforation especially when overlapping with indomethacin).
• They are not first-line prevention; caffeine, gentle ventilation, and nutrition are.
• If a course is ordered, watch glucose (many neonates drift above 150–180 mg/dL on steroids), blood pressure, and gut signs, and do not stop a taper because an afternoon saturation looked pretty.

Exam traps: calling every oxygen day after 28 weeks “BPD” without the 36-week PMA idea; treating PIE with more PIP; claiming vitamin A or PDA ligation “cures” BPD; and inventing a steroid recipe as if it were handbook law.

Independent mixed-item practice is at /practice/ccrn-neonatal.